What is the primary mode of action of tetracycline antibiotics?

Tetracycline antibiotics primarily act by inhibiting protein synthesis, specifically by binding to the 30S ribosomal subunit of bacterial ribosomes. This binding prevents the attachment of aminoacyl-tRNA to the ribosomal acceptor (A) site, effectively blocking the initiation of protein translation. As a result, the synthesis of essential proteins required for bacterial growth and reproduction is halted. This mechanism is particularly effective against a broad range of Gram-positive and Gram-negative bacteria, making tetracyclines versatile in treating various infections.

Other mechanisms of action listed do not pertain to tetracyclines. They do not disrupt cell wall synthesis, which is the primary action of antibiotics like penicillins and cephalosporins. Tetracyclines also do not inhibit DNA replication, as quinolones and other classes of antibiotics do. Furthermore, they do not interfere with metabolic pathways in the same manner as sulfonamides or isoniazid. The specific targeting of the ribosomal subunit allows tetracyclines to remain effective against bacteria while minimizing the impact on human cells, which rely on a different ribosomal structure.